Larsen CH, Bendstrup E, Neergaard MA. Screening Tools for Depression and Anxiety in Patients with Chronic Obstructive Pulmonary Disease – A Systematic Review. COPD. 2021 Dec;18(6):683-689. doi: 10.1080/15412555.2021.1972091. Epub 2021 Sep 5. PMID: 34486457.
Burki TK. Volcanic eruption in Tonga and effects on respiratory health. Lancet Respir Med. 2022 Feb 9:S2213-2600(22)00054-6. doi: 10.1016/S2213-2600(22)00054-6. Epub ahead of print. PMID: 35150609.
Antimicrobial Resistance Collaborators. Global burden of bacterial antimicrobial resistance in 2019: a systematic analysis. Lancet. 2022 Feb 12;399(10325):629-655. doi: 10.1016/S0140-6736(21)02724-0. Epub 2022 Jan 19. PMID: 35065702.
Antoniou KM, Vasarmidi E, Russell AM, Andrejak C, Crestani B, Delcroix M, Dinh-Xuan AT, Poletti V, Sverzellati N, Vitacca M, Witzenrath M, Tonia T, Spanevello A. European Respiratory Society Statement on Long COVID-19 Follow-Up. Eur Respir J. 2022 Feb 10:2102174. doi: 10.1183/13993003.02174-2021. Epub ahead of print. PMID: 35144991.
RECOMMENDED BY ANTONIO SPANEVELLO
Patients diagnosed with COVID-19 associated with SARS-CoV-2 infection frequently experience symptom burden post-acute infection or post-hospitalisation. We aim to identify optimal strategies for follow-up care that may positively impact the patient’s quality-of-life (QOL).A European Respiratory Society (ERS) Task Force (TF) convened and prioritised eight clinical questions. A targeted search of the literature defined the timeline of long COVID-19 as one to six months post infection and identified clinical evidence in the follow-up of patients. Studies meeting the inclusion criteria report an association of characteristics of acute infection with persistent symptoms, thromboembolic events in the follow-up period and evaluations of pulmonary physiology and imaging. Importantly, this statement reviews QOL consequences, symptom burden, disability and home care follow-up. Overall, the evidence for follow-up care for patients with long COVID-19 is limited.
Badi YE, Pavel AB, Pavlidis S, Riley JH, Bates S, Kermani NZ, Knowles R, Kolmert J, Wheelock CE, Worsley S, Uddin M, Alving K, Bakke PS, Behndig A, Caruso M, Chanez P, Fleming LJ, Fowler SJ, Frey U, Howarth P, Horváth I, Krug N, Maitland-van der Zee AH, Montuschi P, Roberts G, Sanak M, Shaw DE, Singer F, Sterk PJ, Djukanovic R, Dahlen SE, Guo YK, Chung KF, Guttman-Yassky E, Adcock IM; U-BIOPRED Study Group. Mapping atopic dermatitis and anti-IL-22 response signatures to type 2-low severe neutrophilic asthma. J Allergy Clin Immunol. 2022 Jan;149(1):89-101. doi: 10.1016/j.jaci.2021.04.010. Epub 2021 Apr 20. PMID: 33891981.
RECOMMENDED BY GE SENNA
Background: Transcriptomic changes in patients who respond clinically to biological therapies may identify responses in other tissues or diseases.
Objective: We sought to determine whether a disease signature identified in atopic dermatitis (AD) is seen in adults with severe asthma and whether a transcriptomic signature for patients with AD who respond clinically to anti-IL-22 (fezakinumab [FZ]) is enriched in severe asthma.
Methods: An AD disease signature was obtained from analysis of differentially expressed genes between AD lesional and nonlesional skin biopsies. Differentially expressed genes from lesional skin from therapeutic superresponders before and after 12 weeks of FZ treatment defined the FZ-response signature. Gene set variation analysis was used to produce enrichment scores of AD and FZ-response signatures in the Unbiased Biomarkers for the Prediction of Respiratory Disease Outcomes asthma cohort.
Results: The AD disease signature (112 upregulated genes) encompassing inflammatory, T-cell, TH2, and TH17/TH22 pathways was enriched in the blood and sputum of patients with asthma with increasing severity. Patients with asthma with sputum neutrophilia and mixed granulocyte phenotypes were the most enriched (P < .05). The FZ-response signature (296 downregulated genes) was enriched in asthmatic blood (P < .05) and particularly in neutrophilic and mixed granulocytic sputum (P < .05). These data were confirmed in sputum of the Airway Disease Endotyping for Personalized Therapeutics cohort. IL-22 mRNA across tissues did not correlate with FZ-response enrichment scores, but this response signature correlated with TH22/IL-22 pathways.
Conclusions: The FZ-response signature in AD identifies severe neutrophilic asthmatic patients as potential responders to FZ therapy. This approach will help identify patients for future asthma clinical trials of drugs used successfully in other chronic diseases.
Keywords: Fezakinumab; IL-22; atopic dermatitis; gene set variation analysis; severe asthma
Seys SF, Long MB. The quest for biomarkers in asthma: challenging the T2 versus non-T2 paradigm. Eur Respir J. 2022 Feb 17;59(2):2102669. doi: 10.1183/13993003.02669-2021. PMID: 35177484.
Bradding P. Mechanisms of Mast Cell Activation in Severe Asthma: Beyond IgE. Am J Respir Crit Care Med. 2022 Feb 15;205(4):375-377. doi: 10.1164/rccm.202110-2322ED. PMID: 34856107.
Gevaert P, Bachert C, Maspero JF, Cuevas M, Steele D, Acharya S, Altman P. Phase 3b randomized controlled trial of fevipiprant in patients with nasal polyposis with asthma (THUNDER). J Allergy Clin Immunol. 2022 Jan 27:S0091-6749(21)02599-9. doi: 10.1016/j.jaci.2021.12.759. Epub ahead of print. PMID: 35094848.
Background: Chronic rhinosinusitis with nasal polyps (CRSwNP) is associated with asthma, particularly of late onset. Current treatment options for CRSwNP have limitations, and there is an unmet need for other safe and effective therapies.
Objective: The aim of the THUNDER study was to determine the efficacy and safety of the prostaglandin D2 receptor 2 (DP2) antagonist fevipiprant in patients with CRSwNP and concomitant asthma, measured by improvement in nasal polyp score (primary end point), nasal congestion score, Sinonasal Outcome Test 22 score, and University of Pennsylvania Smell Identification Test score.
Methods: THUNDER was a phase 3b, randomized, multicenter, double-blind, placebo-controlled, parallel-group, 16-week study of fevipiprant 150 mg or 450 mg once daily versus placebo. All patients received intranasal mometasone furoate 200 μg daily.
Results: Ninety-eight patients were randomly assigned to fevipiprant 150 mg (n = 32), fevipiprant 450 mg (n = 34), or placebo (n = 32). Mean (SE) change from baseline in nasal polyp score at week 16 was 0.20 (0.224) for fevipiprant 150 mg, -0.10 (0.216) for fevipiprant 450 mg, and 0.14 (0.233) for placebo. Mean treatment difference was 0.05 (95% confidence interval, -0.59, 0.70; adjusted P = .979) for fevipiprant 150 mg versus placebo and -0.25 (95% confidence interval, -0.88, 0.39; adjusted P = .656) for fevipiprant 450 mg versus placebo. There was no meaningful difference in the secondary end points for fevipiprant versus placebo.
Conclusions: THUNDER provided no evidence of a role for fevipiprant in the treatment of patients with CRSwNP and asthma; future studies may establish a role for other DP2 antagonists, specifically in patients with aspirin-exacerbated respiratory disease.
Keywords: DP(2) receptor; Nasal polyposis; asthma; chronic rhinosinusitis; chronic rhinosinusitis with nasal polyps; fevipiprant; nasal polyps